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COLD AGGLUTININ PADA PENDERITA COMMUNITY ACQUIRED PNEUMONIA Johanis Johanis; Juli Soemarsono
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 18, No 3 (2012)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v18i3.379

Abstract

Cold agglutinins at below physiologic body temperature can cause spontaneous agglutinations of erythrocytes. Cold agglutinins result from a particular antibodies activation on erythrocytes associated with a primary disease, including infection. The generation of antibody activates complement resulting in hemolysis. A 63-year-old man suffered from shortness of breath accompanied with productive cough, fever, right chest pain, loss of appetite, nausea, and occasionally vomiting. Physical examination showed an increase of pulse rate, respiration rate, and body temperature. Lung examination showed right intercostals retraction and rales in both lungs, but no abnormality detected in other organs. Chest X-ray showed pneumonia. EDTA whole blood showed spontaneous agglutinations at room temperature, however this did not occur by maintaining temperature at 37° C. Different complete blood count results were shown between agglutinated blood and absent of agglutination blood samples. As anti-I, anti-i, and/or anti-H was suspected, agglutinations for anti-A and anti-AB occurred by using ABO forward grouping test, whereas reverse grouping showed agglutinations for A, B, and O cells. Protein electrophoresis showed increase of alpha- 1 and gamma globulin; decrease of renal function; slightly increase of indirect bilirubin; and suspected Extended Spectrum Beta-Lactamase (ESBL) Klebsiella pneumoniae. The diagnosis of this case was community acquired pneumonia and suspected ESBL. Cold agglutinins affected CBC evaluations mostly shown in the erithrocyte index, nevertheless this could prevented by maintaining at physiologic body temperature. Infection could induce activation of cold agglutinins.
PATOGENESIS dan PEMERIKSAAN LABORATOPRIUM MIELOFIBROSIS PRIMER Johanis Johanis; Arifoel Hajat
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 17, No 2 (2011)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v17i2.1025

Abstract

Primary myelofibrosis (PMF) is a neoplastic hematologic disease, characterized by clonal hemapoietic stem cell and collagenaccumulation in bone marrow. PMF is not related with underlying myeloproliferative disorders or other diseases. The features of PMFshow marrow fibrosis, megakaryocytes and granulocytes proliferation, and extramedullary hemapoiesis. PMF is classified as BCR-ABLnegativemyeloproliferative disorders. Diagnosis of PMF is based on clinical symptoms of splenomegaly and myelopthisis; bone marrowbiopsy shows granulocytes/megakaryocytes hyperplasia, megakaryocytes dysmorphic and fibrosis; cytogenic testing for mutation ofJAK2V617F+, MPLW5I5L/K+ and BCR-ABL. The diagnostic criterion according to the 2008 WHO classification considers major andminor crieria. The primary purpose for treatment is to improve the quality of life by paliative tratment. The five year survival of PMFpatients is low.
INFEKSI HUMAN IMMUNODEFICIENCY VIRUS (HIV) PADA BAYI DAN ANAK Johanis Johanis; Endang Retnowati
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 18, No 1 (2011)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v18i1.359

Abstract

HIV is an obligate intracellular RNA virus which fully replicates in the host cells notably express CD4+ receptor, such as CD4+ Tlymphocytes, astrocytes, microglias, monocyte-macrophages, Langerhans cells, dendritic cells. There are two types of HIV: HIV-1 and HIV-2. HIV-2 is less pathogenic and less contribution in children. In the developing countries the total number children with HIV increased higher than in the developed countries. HIV infection in children is more common in children who have HIV infected mothers, they are mostly transmitted during the laboring process. Breast milk from HIV infected mothers is a potential transmission media, there fore HIV infected mothers is not admitted giving breast milk to their babies. The risk factors of mother-child transmissions of HIV infection are: virus, maternal, obstetric, fetal and baby. Maternal HIV antibodies in child’s circulation cause the diagnosis of HIV in children difficult. There fore an accurate and fast diagnosis is needed to decrease the disease progressivity in children as well as by proper antiretroviral treatment. There are suggestion reference for diagnosis tests for HIV infection in babies and children <18 months by virology test using HIV-DNA PCR and HIV-RNA PCR. The diagnosis test for children ≥18 is HIV antibody test the same such as in adult. In HIV infected babies and children is used CD4+ T-lymphocytes percentage to monitor the disease progressivity.
DIAGNOSTIC OF C-REACTIVE PROTEIN IN FEBRILE CHILDREN Johanis Johanis; Aryati Aryati; Dominicus Husada; Djoko Marsudi; M. Y. Probohoesodo
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 18, No 2 (2012)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v18i2.1010

Abstract

The measurement of C-reactive protein (CRP), an acute-phase protein synthesized by hepatocytes, is valuable to distinguish bacterialinfection from non-bacterial infections in children. The aim of this study is to know the diagnostic properties of quantitative CRPassociated with clinically bacterial and non-bacterial infection in febrile children. Febrile children which was studied were presentingin the Paediatric Emergency Department, their ages were up to 12 years, with axillary’s temperature ≥38.5° C, and the clinicallyundetectable source of fever were enrolled in this consecutive study from September, 2009, up to August, 2010. Informed consent wasobtained for the use of CRP evaluation. The CRP concentration was measured with immunoturbidimetry method (Pure auto S CRP latex(SS-type), Sekisui Medical Co., Ltd) and an auto photometer TMS 1024i. The main outcome result was the presence of the laboratoryexamination results, blood culture, or radio graphically. The receiver operator characteristic (ROC) curve was modelled for quantitativeCRP to identify the optimal test value. Eighty-six patients were enrolled in this study. Forty-one (47.6%) had bacterial infection and 45(52.3%) had non-bacterial infection. The CRP concentration was significantly different between the two groups (p=0.003). The ROCanalysis demonstrated an area under curve (AUC) 0.689, standard error (SE) 0.059, and 95% confidence interval (CI): 0.573-0.805.The optimal cut-off point for CRP in this data set at 5 mg/L, achieved sensitivity of 0.61, specificity of 0.71, and likelihood ratio 2.11(Kappa 0.003, McNemar 0.711) for the detection of bacterial infection in this population. The Quantitative CRP concentration is avaluable laboratory test for the evaluation of febrile children who are at risk of bacterial infection.